THE EXTRAPYRAMIDAL MOTOR SYSTEM 



885 



it and the nucleus ruber. They probably interrupt 

 at least partially the ascending efferent fibers from 

 the nucleus niger. According to VVhittier & Mettler 

 (293), their lesions responsible for a static tremor are 

 located more rostrally and dorsally to the substantia 

 nigra. 



Observations from human pathology are particu- 

 larly important here since experiments in animals do 

 not give definite information concerning the func- 

 tional significance of the nucleus niger. On the basis 

 of three cases with localized lesions, Brissaud (14) 

 was the first to assert that destruction of the nucleus 

 niger is responsible for parkinsonism. The later ob- 

 servations of Tretiakoff (258), Foix (59) and Spatz 

 (237) pointed to the nucleus niger as being the site 

 of major damage in postencephalitic parkinsonism. 

 Genuine paralysis agitans is also due to cell destruc- 

 tion specifically localized in the nucleus niger [Hassler 

 (79)]. The tremor (without rigor and akinesia), 

 in the contrary, is caused by a diffuse lesion (elat 

 precible) of the striatum [Hassler (80)]. Rigor and 

 akinesia, the two other motor components of parkin- 

 sonism, are caused by lesions in the nucleus niger, 

 mainly in its posterior portion. In most patients with 

 this disorder significant pallidum lesions are missing 

 [Hassler (79), Klaue (149)]- 



The mechanisms of resting tremor, akinesia and 

 rigidity are now better understood as a result of the 

 stereotaxic operations which have recently been 

 performed on patients suffering from parkinsonian 

 disorders. In 181 7 James Parkinson had already 

 described the disappearance of resting tremor follow- 

 ing a subsequent hemiplegia. Bucy (20, 22, 25) could 

 very definitely reduce or even abolish the resting 

 tremor by resection of the arm area in the precentral 

 gyrus and of area 4 gamma. The same effect was ob- 

 tained by Putnam (215) following unilateral 

 pyramidotomy in the spinal cord. In both cases the 

 effect was associated with a contralateral hemiparesis. 

 The tremor reappeared as soon as the paresis dis- 

 appeared. Hence it must be concluded that the tremor 

 depends upon a facilitatory influence of the pyramidal 

 tract on the anterior horn mechanisms. .\. continuous 

 flow of subliminal pyramidal impulses influencing 

 anterior horn cells has been demonstrated electro- 

 physiologically by Adrian & Moruzzi (i). The tremor 

 frequency, however, is not the same as the spontaneous 

 rhythmic activity of the cortical motor areas [Schwab 

 & Cobb (230), Jung (130)]. Its rhythm probably is 

 not produced by cerebral mechanisms but by bulbo- 

 spinal interneurons; it is thus understandable that 



the ipsilateral tremor is rarely synchronous in arm and 

 leg [Jung (130)]. 



In an effort to suppress the pyramidal facilitation 

 of the tremor without producing a hemiparesis, 

 Hassler and associates destroyed stereotaxically the 

 nucleus ventro-oralis posterior of patients with 

 Parkinson's disease. This was intended to abolish the 

 afferent inflow from this nucleus to area 47 of the 

 cortex, while leaving the efferent pyramidal path 

 intact. The result was a definite decrease or even 

 suppression of the contralateral resting tremor. If 

 the tremor temporarily disappears before coagulation, 

 it can be evoked by low-frequency stimulation of the 

 nucleus V.o.p. ; if the tremor persists, it may be en- 

 hanced, accelerated or blocked by such stimulation. 

 Single shocks enhance the momentary phase of the 

 tremor which is followed by a compensatory interval 

 in either flexion or extension; stimuli at 4 per sec. 

 slow the tremor, at 8 per sec. they accelerate it, while 

 at higher frequencies it is blocked. Similar but less 

 definite effects may be obtained by stimulating the 

 nucleus ventro-oralis anterior (V.o.a.), which is a 

 terminal nucleus for fibers coming from the internal 

 pallidum (Hi of Forel). Thus, ijipolar stimulation of 

 the internal pallidum also causes similar but less 

 marked changes in the tremor. The internal pallidum 

 projects via V.o.a. to the area 6aa: in the precentral 

 gyrus where many fibers of the pyramidal tract origi- 

 nate. Thus, this part of the afferent pyramidal 

 pathway is also capable of influencing the tremor 

 frequency, although the effect is less marked than 

 that of V.o.p. 



A complete and permanent suppression of the 

 resting tremor seems to result onlv from either a 

 lesion of the pyramidal tract causing a hemiparesis 

 or a lesion of the thalamofrontocortical pathways 

 producing personality changes with decreased emo- 

 tional responsiveness. The emotional enhancement 

 of the resting tremor can be suppressed by prefrontal 

 lobotomy. One may conclude therefore that in 

 parkinsonian disease prefrontal cortical areas exert 

 their descending corticifugal influence during emo- 

 tional stress by means of prefrontoreticular and pre- 

 frontopallidal pathways, and in cases of genuine 

 tremor with an intact nucleus niger also via pre- 

 frontonigral fibers. Definite impro\ement, however, 

 can be produced by coagulation of the oral ventral 

 nuclei of the thalamus (\'.o.a. and V.o.p) or of the 

 pallidum without undesirable side effects (86,88, 90). 



These therapeutic effects provide evidence of 

 facilitatory influences both from afferent and efferent 

 pyramidal pathways and prefrontal systems upon the 



